ORCID Profile
0000-0002-0249-5946
Current Organisation
The University of Notre Dame Australia - Sydney Campus Broadway
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Publisher: Common Ground Research Networks
Date: 2018
Publisher: Informa UK Limited
Date: 04-2016
DOI: 10.1128/MCB.01035-15
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 29-10-2015
Abstract: Tumor necrosis factor–related apoptosis‐inducing ligand ( TRAIL ) has the ability to inhibit angiogenesis by inducing endothelial cell death, as well as being able to promote pro‐angiogenic activity in vitro. These seemingly opposite effects make its role in ischemic disease unclear. Using Trail −/− and wildtype mice, we sought to determine the role of TRAIL in angiogenesis and neovascularization following hindlimb ischemia. Reduced vascularization assessed by real‐time 3‐dimensional Vevo ultrasound imaging and CD 31 staining was evident in Trail −/− mice after ischemia, and associated with reduced capillary formation and increased apoptosis. Notably, adenoviral TRAIL administration significantly improved limb perfusion, capillary density, and vascular smooth‐muscle cell content in both Trail −/− and wildtype mice. Fibroblast growth factor‐2, a potent angiogenic factor, increased TRAIL expression in human microvascular endothelial cell‐1, with fibroblast growth factor‐2‐mediated proliferation, migration, and tubule formation inhibited with TRAIL si RNA . Both fibroblast growth factor‐2 and TRAIL significantly increased NADPH oxidase 4 ( NOX 4) expression. TRAIL ‐inducible angiogenic activity in vitro was inhibited with si RNA s targeting NOX 4, and consistent with this, NOX 4 mRNA was reduced in 3‐day ischemic hindlimbs of Trail −/− mice. Furthermore, TRAIL ‐induced proliferation, migration, and tubule formation was blocked by scavenging H 2 O 2 , or by inhibiting nitric oxide synthase activity. Importantly, TRAIL ‐inducible endothelial nitric oxide synthase phosphorylation at Ser‐1177 and intracellular human microvascular endothelial cell‐1 cell nitric oxide levels were NOX 4 dependent. This is the first report demonstrating that TRAIL can promote angiogenesis following hindlimb ischemia in vivo. The angiogenic effect of TRAIL on human microvascular endothelial cell‐1 cells is downstream of fibroblast growth factor‐2, involving NOX 4 and nitric oxide signaling. These data have significant therapeutic implications, such that TRAIL may improve the angiogenic response to ischemia and increase perfusion recovery in patients with cardiovascular disease and diabetes.
Publisher: Edith Cowan University
Date: 09-2021
DOI: 10.14221/AJTE.2021V46N9.5
Abstract: In Australia, teacher education students must pass the Literacy and Numeracy Test for Initial Teacher Education (LANTITE) to meet accreditation requirements. Although this has been mandated since 2016, there are currently few resources available for students to use in preparation for the test. To help students prepare for the numeracy component of the LANTITE, we developed an online Numeracy Practice Test (NPT) through the institution’s learning management system. This study assessed the learning analytics from the NPT between students who subsequently passed the numeracy component of the LANTITE with those that failed. Our results show that students who passed performed significantly better in the NPT, had fewer attempts, spent less time on the NPT, and accessed it closer to the date of the LANTITE, which demonstrate students’ ability to self-assess the level of support required.
Publisher: Wiley
Date: 15-09-2016
Publisher: Elsevier BV
Date: 04-2021
Publisher: University of Otago Library
Date: 22-11-2016
Publisher: Elsevier BV
Date: 05-2021
DOI: 10.1016/J.PHARMTHERA.2020.107711
Abstract: Myeloperoxidase (MPO) is a prominent mammalian heme peroxidase and a fundamental component of the innate immune response against microbial pathogens. In recent times, MPO has received considerable attention as a key oxidative enzyme capable of impairing the bioactivity of nitric oxide (NO) and promoting endothelial dysfunction a clinically relevant event that manifests throughout the development of inflammatory cardiovascular disease. Increasing evidence indicates that during cardiovascular disease, MPO is released intravascularly by activated leukocytes resulting in its transport and sequestration within the vascular endothelium. At this site, MPO catalyzes various oxidative reactions that are capable of promoting vascular inflammation and impairing NO bioactivity and endothelial function. In particular, MPO catalyzes the production of the potent oxidant hypochlorous acid (HOCl) and the catalytic consumption of NO via the enzyme's NO oxidase activity. An emerging paradigm is the ability of MPO to also influence endothelial function via non-catalytic, cytokine-like activities. In this review article we discuss the implications of our increasing knowledge of the versatility of MPO's actions as a mediator of cardiovascular disease and endothelial dysfunction for the development of new pharmacological agents capable of effectively combating MPO's pathogenic activities. More specifically, we will (i) discuss the various transport mechanisms by which MPO accumulates into the endothelium of inflamed or diseased arteries, (ii) detail the clinical and basic scientific evidence identifying MPO as a significant cause of endothelial dysfunction and cardiovascular disease, (iii) provide an up-to-date coverage on the different oxidative mechanisms by which MPO can impair endothelial function during cardiovascular disease including an evaluation of the contributions of MPO-catalyzed HOCl production and NO oxidation, and (iv) outline the novel non-enzymatic mechanisms of MPO and their potential contribution to endothelial dysfunction. Finally, we deliver a detailed appraisal of the different pharmacological strategies available for targeting the catalytic and non-catalytic modes-of-action of MPO in order to protect against endothelial dysfunction in cardiovascular disease.
Publisher: Springer Singapore
Date: 15-09-2016
Publisher: SAGE Publications
Date: 23-08-2023
DOI: 10.1177/10538259231193730
Abstract: Background: The literature has expounded on the impacts of international service-learning (ISL) in teacher education as positively affecting everything from improving academic achievement to developing a greater moral and ethical sense. Other studies have examined the role of cultural competence and dimensions of power between those providing and receiving service. Purpose: This paper examines a decade-long ISL immersion program to understand the outcomes on students in three key areas that have received attention in the literature: motivation, employment, and academics. Methodology: A longitudinal case study comprising a cross-section of students who were asked to reflect on their immersion experiences, which took place from 2011 to 2020. Reflective journals completed during and directly after each immersion supplemented the survey data. Findings: While much of the data supports previous studies regarding the impacts of ISL, there are some anomalous findings, especially in the longer-term effects of ISL within teacher education. While participants’ perceptions of the impacts were significant, evidence of that impact was lacking. Implications: Although short-term impacts of the immersion were more significantly noted, students perceived the impact for more extended periods than previously thought. However, the evidence to suggest that these perceptions are realizable is lacking.
Publisher: The WAC Clearinghouse; University Press of Colorado
Date: 15-10-2020
Publisher: The Company of Biologists
Date: 15-07-2015
DOI: 10.1242/BIO.011494
Abstract: During embryonic development, hematopoietic cells develop by a process of endothelial-to hematopoietic transition of a specialized population of endothelial cells. These hemogenic endothelium (HE) cells in turn develop from a primitive population of FLK1+ mesodermal cells. Endoglin (ENG) is an accessory TGF-β receptor that is enriched on the surface of endothelial and hematopoietic stem cells and is also required for the normal development of hemogenic precursors. However, the functional role of ENG during the transition of FLK1+ mesoderm to hematopoietic cells is ill defined. To address this we used a murine embryonic stem cell model that has been shown to mirror the temporal emergence of these cells in the embryo. We noted that FLK1+ mesodermal cells expressing ENG generated fewer blast colony-forming cells but had increased hemogenic potential when compared with ENG non-expressing cells. TIE2+/CD117+ HE cells expressing ENG also showed increased hemogenic potential compared with non-expressing cells. To evaluate whether high ENG expression accelerates hematopoiesis, we generated an inducible ENG expressing ES cell line and forced expression in FLK1+ mesodermal or TIE2+/CD117+ HE cells. High ENG expression at both stages accelerated the emergence of CD45+ definitive hematopoietic cells. High ENG expression was associated with increased pSMAD2/eNOS expression and NO synthesis in hemogenic precursors. Inhibition of eNOS blunted the ENG induced increase in definitive hematopoiesis. Taken together, these data show that ENG potentiates the emergence of definitive hematopoietic cells by modulating TGF-β SMAD2 signalling and increasing eNOS/NO synthesis.
Location: Australia
No related grants have been discovered for Thuan Thai.